Gingivitis

Def: Inflammation of gingiva without clinical attachment loss

Classification

1. Dental plaque induced gingival disease

• Gingivitis associated with dental plaque only
• Gingival disease modified by systemic factors
• Gingival disease modified by medications
• Gingival disease modified by malnutrition

2. Non plaque induced gingival lesion

• Those of bacterial, viral, fungal origin
• Genetic origin
• Systemic origin
• Trauma
• Foreign body reactions

Plaque

Def: Aggregate of microorganisms – in which cells produce extracellular matrix – and are adherent to each other – and onto the tooth surface

Steps on plaque formation:

1. Association – Dental pellicle forms
2. Adhesion – Bacteria bind onto pellicle within hours
3. Proliferation – of bacteria
4. Microcolony formation
5. Biofilm formation – Formation of symbiotic relationship
6. Growth & maturation – Biofilm develops primitive circulatory system

Risk factors:

2. External/acquired

• Alcohol
• Drugs
• Smoking
• Stress
• Medication use

3. Local

• Poor oral hygiene
• Poor restoration – overhang/defective
• Increased calculus
• Areas subjected to food impaction
• Carious lesions and margins

Factors contributing to severity:

• Pathogenic bacteria
• Environmental factors
• Genetic factors

Healthy gingiva:

• Stippling gingiva, knife edge (interdental papilla), symmetrical distribution of pigment

---

Periodontitis

Def: Inflammation of supporting tissues of the teeth with clinical attachment loss

Clinical classification

1. Prepubertal (accelerated) periodontitis – Rare, genetic/medical condition

• Affects deciduous dentition
• Extensive destruction of alveolar bone
• Associated with systemic disease – Affects neutrophils:
  • 1. Neutrophil abnormality:
    • Agranulocytosis (↑M, ↑Lymph)
    • Neutropenia (↓N)
  • 2. Neutrophil dysfunction:
    • Down’s syndrome
    • Juvenile DM
    • Papillon – Lefevre syndrome
  • 3. Other systemic dx:
    • Hypophosphatasia
    • Histiocytosis X
    • Ehler-Danlos VIII

2. Juvenile Periodontitis – Uncommon, puberty & adolescence

• More in females
• Clinical presentation – Rapid destruction of alveolar bone. Starts with central incisors & first molars
• Etiology: Bacteria
  • Actinobacillus actinomycetemcomitans
  • Capnocytophagea
  • Eikenella corrodens

3. Rapidly progressive/ aggressive – Uncommon, late adolescence

• From puberty to 30 years of age
• Affects entire dentition (1ry and 2ry)
• Etiology: Leukocyte dysfunction

4. Chronic adult periodontitis – Common, adults over 30

• Chronic bacterial destruction + plaque + calculus deposits

Chronic adult periodontitis

– Evidence of CAP is of bacterial origin:

1. Epidemiological studies – +ve association between dental plaque & PDL disease
2. Clinical experiment – No oral hygiene – plaque and gingivitis present
3. Topical antimicrobials eliminate disease
4. Isolate pathological bacteria from bacterial pocket
5. Bacteria from plague cause disease in gnotobiots

– Systemic factors that cause disease progression:

Pathogenesis of PDL disease

Progression depends on balance between host & microbial factors

Host factors:

1. Salivary factors
2. Epithelial barrier
3. Crevicular fluid
4. Immune response
5. Transmigrating neutrophils
6. Tissue regeneration & repair

Microbial factors:

1. Direct injury
2. Toxic products
3. Enzymes
4. Antigenic challenge

Disturbance in host – parasite relationship leads to:

1. Activation of host immune & inflammatory response
2. ↑ Synthesis of inflammatory mediators & cytokines (IL-1, IL-6)
3. Breakdown of CT and bone resorption
4. Progression of PDL disease

Clinical progression of PDL disease

1. Initial lesion: 2-4 days, base of gingival sulcus. Gingivitis

• Acute inflammation:
  • Vasodilation
  • Crevicular fluid exudates
  • PMN infiltrates
  • Neutrophil and monocytes appear
• Disruption of junctional epithelium

2. Early lesion: 4-7 days, exacerbation of initial gingivitis

• Change in junctional epithelium:
  • Disruption of intercellular spaces
  • Detachment from enamel
  • Deepening of gingival sulcus
  • Subgingival plaque formation
• Lymphocytic infiltrate
• Loss of collagen
• Hyperplastic junctional epithelium (JE)
• Damage fibroblast cell membrane & organelles

3. Established lesion: 2-3 weeks, disrupt JE. Gingivitis

• Ulceration of gingival pocket epithelium – plasma cell infiltrate
• Destruction of gingival CT – expansion of involved tissues
• Hyperplastic gingivitis (repair)

4. Advanced lesion: Periodontitis – 3 weeks – inflammation spreads to alveolar bone & PDL

• Destruction of CT:
  • Collagen degradation
  • Bone resorption
  • Pocket formation
• 50% plasma cells
• Clinical attachment loss (CAL) > 3mm

– Mechanism of degradation of CT and collagen:

1. Cytopathic changes in fibroblasts – ↓ synthetic activity
2. ↑ enzyme activity of:
   • Collagenase (produced by bacteria & fibroblast)
   • Metalloproteinases (inflam. cytokines)
   • Other proteases

– Pathological features of established PDL disease:

1. Persistent gingivitis
2. Loss of CT attachment
3. Destruction of alveolar bone
4. Predominance of plasma cells
5. Apical extension of destructive inflammation
6. Healing with periods of quiescence

Long term effects of apical periodontitis

• Apical periodontitis: Tender on mastication, edema and inflammation in pdl. Widened pdl due to bone resorption in x-ray.

Other periodontal conditions

1. Lateral PDL abscess

Localized area of pus in PDL pocket

• Acute:
  • Develops rapidly
  • Redness, swelling, tenderness of overlying mucosa
  • Throbbing pain
• Chronic – dull pain/ asymptomatic

Picture

2. Pericoronitis

• Pain
• Bad taste
• Pus discharge
• Tender gum flap

Acute pericoronitis – Common site – 7 & 8

• Pain
• Trismus (lock jaw)
• Fever
• Hyperemia
• lymphadenitis
• Swelling
• Halitosis

• Tx: Antibiotics, operculectomy, disimpaction

Picture

3. Acute necrotizing gingivitis

Disease of young people

Etiology:

• Borrelia vincentii
• Fusiform bascilli

Clinical presentation:

• Interdental papillae ulcers
• Gingival bleeding
• Halitosis
• Sialorrhoea (drooling)

Predisposing feature:

• Respiratory infection
• Poor oral hygiene
• Smoking
• Immunodeficiency & HIV
• Malnutrition

Picture

4. NOMA/ Cancrum oris/ Gangrenous stomitis

• Rapidly progressive, polymicrobial, opportunistic infection – leads to destruction of orofacial tissues
• Malnourished children

Etiology:

• Borrelia vincentii
• Staph. aureus
• Prevotella intermedia
• Fusobacterium necrophorum

Underlying systematic disease:

• Malnutrition, poverty
• Dehydration
• Poor oral hygiene
• Burkitt’s lymphoma
• HIV
• Leukemia
• Noma neonatorum – low birth weight, premature ill infants
• Debilitating childhood disease
• Pneumonia
• Sepsis
• Oral mucosal ulcers
• Trauma
• Acute necrotizing gingivitis – antecedent lesion

Clinical presentation:

• Tissue necrosis
• Painful ulcers on gingiva/ buccal mucosa
• Rapidly spreading – cause necrosis
• Fetid odor
• Exfoliated teeth
• Sequestration

Complication:

• Sequestration of involved bone
• Soft tissue necrosis
• Keloid formation
• Microstomia and micrognathia

Management:

• Treat systemic disease
• Rehydrate
• Antibiotics
• Debridement of necrotic tissue
• Reconstructive surgery

Picture

---

Generalized enlargement of gingiva:

1. Local factors – Plaque, calculus, bacteria
2. Hormonal imbalance – Estrogen, progesterone, vit C deficiency
   • Pregnancy, puberty, pills
3. Systemic disease – Leukemia, Wegener’s granulomatosis
4. Genetic factors – Cowden syndrome (multiple oral papilloma)
5. Drugs – Phenytoin, cyclosporin, nifedipine, verapamil
6. Gingival fibromatosis
7. Chronic hyperplastic gingivitis

Clinical presentation:

• Increased bulk of gingiva
• Loss of stippling
• Gingival margins rolled & blunted
• Red-blue if inflamed

Histology:

• Abundant collagen
• Scanty fibroblasts
• Inflammatory infiltrate
• Leukemia – atypical & immature WBC

Management:

• Gingivectomy/ gingivoplasty
• Prophylaxis
• OHI (Oral hygiene instructions)

Picture